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NursIII T1key points
Nursing III Test 1 key points
| Question | Answer |
|---|---|
| Chapter 48: | Nursing Assessment: Endocrine System |
| Hormones exert their effects | on target tissue. |
| The specificity of hormone–target cell interaction | is determined by receptors in a “lock-and-key” type of mechanism. |
| The regulation of hormone levels in the blood depends on | a highly specialized mechanism called feedback. |
| With negative feedback, the gland responds by increasing or decreasing the secretion of | a hormone based on feedback from various factors. |
| The hypothalamus and pituitary gland integrate | communication between the nervous and endocrine systems. |
| Several hormones secreted by the anterior pituitary are referred to as | tropic hormones because they control the secretion of hormones by other glands. |
| Thyroid-stimulating hormone (TSH) | stimulates the thyroid gland to secrete thyroid hormones. |
| Adrenocorticotropic hormone (ACTH) | stimulates the adrenal cortex to secrete corticosteroids. |
| Follicle-stimulating hormone (FSH) | stimulates secretion of estrogen and the development of ova in the female and sperm development in the male. |
| Luteinizing hormone (LH) | stimulates ovulation in the female and secretion of sex hormones in both the male and female. |
| Growth hormone (GH) | has effects on all body tissues. |
| Antidiuretic hormone (ADH) | regulates fluid volume by stimulating reabsorption of water in the kidneys. |
| Oxytocin | stimulates ejection of milk into mammary ducts and contraction of uterine smooth muscle. |
| The major function of the thyroid gland | is the production, storage, and release of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). |
| Iodine | is necessary for the synthesis of thyroid hormones. |
| T4 and T3 | affect metabolic rate, carbohydrate and lipid metabolism, growth and development, and nervous system activities. |
| Calcitonin | is a hormone produced by C cells (parafollicular cells) of the thyroid gland in response to high circulating calcium levels. |
| The parathyroid glands | are four small, oval structures usually arranged in pairs behind each thyroid lobe. |
| parathyroid hormone (PTH) | regulates the blood level of calcium. |
| The adrenal glands | are small, paired, highly vascularized glands located on the upper portion of each kidney. |
| The adrenal medulla secretes the catecholamines | epinephrine (the major hormone [75%]), norepinephrine (25%), and dopamine. |
| The adrenal cortex | secretes cortisol, which is the most abundant and potent glucocorticoid. |
| Cortisol is necessary | to maintain life. Its functions include regulation of blood glucose concentration, inhibition of inflammatory action, and support in response to stress. |
| Aldosterone | is a potent mineralocorticoid that maintains extracellular fluid volume. |
| The adrenal cortex | secretes small amounts of androgens. Adrenal androgens stimulate pubic and axillary hair growth and sex drive in females. |
| The pancreas | secretes several hormones, including glucagon and insulin. |
| Glucagon | increases blood glucose by stimulating glycogenolysis, gluconeogenesis, and ketogenesis. |
| Insulin | is the principal regulator of the metabolism and storage of ingested carbohydrates, fats, and proteins. |
| Normal aging results in | decreased hormone production and secretion, altered hormone metabolism and biologic activity, decreased responsiveness of target tissues to hormones, and alterations in circadian rhythms. |
| Subtle changes of aging often mimic | manifestations of endocrine disorders. |
| Hormones affect every body tissue and system, | causing great diversity in the signs and symptoms of endocrine dysfunction. |
| Endocrine dysfunction | may result from deficient or excessive hormone secretion, transport abnormalities, an inability of the target tissue to respond to a hormone, or inappropriate stimulation of the target-tissue receptor. |
| Subjective data: | The nurse should inquire about use of hormone replacements, previous hospitalizations, surgery, chemotherapy, and radiation therapy (especially of the neck). |
| Objective data: | Most endocrine glands are inaccessible to direct examination. |
| Physical examination: | Clinical manifestations of endocrine function vary significantly, depending on the gland involved. |
| Assessment includes | a history of growth and development, weight distribution and changes, and comparisons of these factors with normal findings. |
| Disorders can commonly cause | changes in mental and emotional status. |
| The nurse should note the color and texture | of the skin, hair, and nails. The skin should be palpated for skin texture and presence of moisture. |
| When inspecting the thyroid gland, | observation should be made first in the normal position (preferably with side lighting), then in slight extension, and then as the patient swallows some water. |
| The thyroid | is palpated for its size, shape, symmetry, and tenderness and for any nodules. |
| The size, shape, symmetry, and general proportion | of hand and feet size should be assessed. |
| The hair distribution | pattern of the genitalia should be inspected. |
| DIAGNOSTIC STUDIES | Laboratory tests usually involve blood and urine testing. |
| Ultrasound may be used as a screening tool | to localize endocrine growths such as thyroid nodules. |
| Laboratory studies may include | direct measurement of the hormone level, or involve an indirect indication of gland function by evaluating blood or urine components affected by the hormone (e.g., electrolytes). |
| Notation of sample time on the laboratory slip and sample | is important for hormones with circadian or sleep-related secretion. |
| The studies used to assess function of the anterior pituitary hormones relate to | GH, prolactin, FSH, LH, TSH, and ACTH. |
| Tests to assess abnormal thyroid function include | TSH (most common), total T4, free T4, and total T3. |
| Chapter 50: | Nursing Management: Endocrine Problems |
| Acromegaly | results from excess secretion of growth hormone (GH).It is a rare condition of bone and soft tissue overgrowth.Bones increase in thickness and width but not length. |
| ACROMEGALY Manifestations include | enlargement of hands and feet, thickening and enlargement of face and head bony and soft tissue, sleep apnea, signs of diabetes mellitus, cardiomegaly, and hypertension. |
| ACROMEGALY Treatment focuses | on returning GH levels to normal through surgery, radiation, and drug therapy. The prognosis depends on age at onset, age when treatment is initiated, and tumor size. |
| ACROMEGALY Nursing care | for surgical patients postoperatively includes avoidance of vigorous coughing, sneezing, and straining at stool to prevent cerebrospinal fluid leakage from where the sella turcica was entered. |
| After surgery with a transsphenoidal approach, | the head of the bed is elevated to a 30-degree angle at all times, and neurologic status is monitored. Mild analgesia is used for headaches, and toothbrushing is avoided for at least 10 days. |
| If hypophysectomy | is done or the pituitary is damaged, antidiuretic hormone (ADH), cortisol, and thyroid hormone replacement must be taken for life. Patient teaching is essential with hormone replacement therapy. |
| Hypopituitarism | is rare, and involves a decrease in one or more of the pituitary hormones: |
| The anterior pituitary gland secretes | adrenocorticotrophic hormone (ACTH), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), GH, and prolactin. |
| The posterior pituitary gland secretes | ADH and oxytocin. |
| Hypopituitarism Most deficiencies associated with hypopituitarism involve | GH and gonadotropins (e.g., LH, FSH) due to a pituitary tumor. |
| Syndrome of inappropriate antidiuretic hormone (SIADH) | results from an overproduction or oversecretion of ADH. |
| SIADH results from | abnormal prod or sustained secretion of ADH&is chara. by fluid retention,serum hypoosmolality,dilutional hyponatremia, hypochloremia,conc urine in presence of normal or inc intravascular volume,normal renal function.most common cause is lung cancer |
| SIADH Treatment | directed @underlying cause,w/goal to restore normal fluid volume &osmolality.Fluid restriction results in gradual,daily weight reductions,progressive rise in serum NA conc &osmolality,symptomatic improvement.chronic SIADH,the pt must learn self-management |
| Diabetes insipidus (DI) | is associated with deficiency of production or secretion of ADH or decreased renal response to ADH. |
| Decreases in ADH cause | fluid and electrolyte imbalances due to increased urinary output and increased plasma osmolality. Depending on the cause, DI may be transient or chronic lifelong condition. |
| Types of DI include: Central DI (or neurogenic DI) | occurs when an organic lesion of the hypothalamus, infundibular stem, or posterior pituitary interferes with ADH synthesis, transport, or release. |
| Nephrogenic DI | occurs when there is adequate ADH, but a decreased kidney response to ADH. Lithium is a common cause of drug-induced nephrogenic DI. Hypokalemia and hypercalcemia may also lead to nephrogenic DI. |
| Psychogenic DI | is associated with excessive water intake, caused by lesion in thirst center or by psychosis. |
| DI is characterized | by polydipsia and polyuria. |
| If oral fluid intake cannot keep up with urinary losses, | severe fluid volume deficit results as manifested by weight loss, constipation, poor tissue turgor, hypotension, and shock. Severe dehydration and hypovolemic shock may occur. |
| DI Treating the primary cause | is central to management. Therapeutic goal is maintenance of fluid and electrolyte balance. |
| DI Nursing care includes | early detection, maintenance of adequate hydration, and patient teaching for long-term management. |
| Goiter is thyroid gland hypertrophy and enlargement caused | by excess TSH stimulation, which can be caused by inadequate circulating thyroid hormones. |
| Goiter | is also found in Graves’ disease. |
| TSH and T4 levels | are measured to determine if goiter is associated with hyperthyroidism, hypothyroidism, or normal thyroid function. |
| Thyroid antibodies | are measured to assess for thyroiditis. |
| Treatment with thyroid hormone | may prevent further thyroid enlargement.Surgery to remove large goiters may be done. |
| A thyroid nodule, | a palpable deformity of the thyroid gland, may be benign or malignant. |
| Benign nodules are usually not dangerous, | but can cause tracheal compression if they become too large. |
| Malignant tumors of thyroid gland | are rare. |
| A major sign of thyroid cancer | is presence of hard, painless nodule or nodules on enlarged thyroid gland. |
| Thyroid Surgical tumor removal | is usually indicated with cancer. |
| Thyroid tumors Procedures | include unilateral total lobectomy with removal of isthmus to total thyroidectomy with bilateral lobectomy. Radiation therapy may also be indicated. |
| Nursing care for thyroid tumors | is similar to care for patient who has undergone thyroidectomy. |
| Thyroiditis | is an inflammatory process in the thyroid gland. |
| Subacute and acute forms of thyroiditis | have abrupt onset, and the thyroid gland is painful. |
| Chronic autoimmune thyroiditis (Hashimoto’s thyroiditis) | can lead to hypothyroidism. |
| Hashimoto’s thyroiditis | is a chronic autoimmune disease in which thyroid tissue is replaced by lymphocytes and fibrous tissue. It is most common cause of goiterous hypothyroidism. Recovery may be complete in weeks or months without treatment. |
| Hyperthyroidism | is thyroid gland hyperactivity with sustained increase in synthesis and release of thyroid hormones. |
| Thyrotoxicosis | refers to physiologic effects or clinical syndrome of hypermetabolism resulting from excess circulating levels of T4, T3, or both. |
| Hyperthyroidism and thyrotoxicosis | usually occur together as in Graves’ disease. |
| The most common form of hyperthyroidism | is Graves’ disease. Other causes include toxic nodular goiter, thyroiditis, exogenous iodine excess, pituitary tumors, and thyroid cancer. |
| Graves’ disease | is an autoimmune disease marked by diffuse thyroid enlargement and excessive thyroid hormone secretion. |
| Factors such as insufficient iodine supply, infection, and stressful life events may interact with genetic factors to cause | Graves’ disease. |
| Graves’ disease Manifestations | relate to the effect of thyroid hormone excess. |
| When thyroid gland is large, a goiter may be noted, and auscultation of thyroid gland | may reveal bruits. |
| A classic finding is exophthalmos, | a protrusion of eyeballs from the orbits. |
| Graves’ disease Treatment | options are antithyroid medications, radioactive iodine therapy, and subtotal thyroidectomy. |
| Thyrotoxic crisis, | also known as thyroid storm, is an acute, rare condition in which all hyperthyroid manifestations are heightened. Although it is a life-threatening emergency, death is rare when treatment is vigorous and initiated early. |
| Thyrotoxic crisis Manifestations | include severe tachycardia, shock, hyperthermia, seizures, abdominal pain, diarrhea, delirium, and coma. |
| Thyrotoxic crisis Treatment | focuses on reducing circulating thyroid hormone levels by drug therapy. |
| Hypothyroidism | is one of most common medical disorders. It results from insufficient circulating thyroid hormone. |
| Hypothyroidism | may be primary (related to destruction of thyroid tissue or defective hormone synthesis), or secondary (related to pituitary disease with decreased TSH secretion or hypothalamic dysfunction with decreased thyrotropin-releasing hormone [TRH] secretion). |
| Hypothyroidism | also can be transient and related to thyroiditis or from a discontinuation of thyroid hormone therapy. Iodine deficiency is the most common cause worldwide. |
| In areas with adequate iodine intake, the most common cause | is thyroid gland atrophy (end result of Hashimoto’s thyroiditis and Graves’ disease). |
| Hypothyroidism Manifestations | include fatigue, lethargy, personality and mental changes, decreased cardiac output, anemia, and constipation. |
| Patients with severe long-standing hypothyroidism may display | myxedema, an accumulation of hydrophilic mucopolysaccharides in dermis and other tissues. This mucinous edema causes characteristic facies of hypothyroidism (i.e., puffiness, periorbital edema, and masklike affect). |
| A myxedema coma | can be precipitated by infection, drugs (opioids,tranquilizers,barbiturates),exposure to cold,trauma. chara by subnormal temp, hypotension,hypoventilation To survive, vital functions are supported and IV thyroid hormone replacement administered. |
| The overall treatment in hypothyroidism | is restoration of euthyroid state as safely and rapidly as possible with hormone replacement therapy. |
| Levothyroxine (Synthroid) | is the drug of choice. |
| Hypothyroidism Patient teaching | is imperative, and the need for lifelong drug therapy is stressed. |
| Hyperparathyroidism | involves increased secretion of parathyroid hormone (PTH).Excess PTH leads to hypercalcemia and hypophosphatemia. |
| Hyperparathyroidism Manifestations | include weakness, loss of appetite, constipation, emotional disorders, and shortened attention span. |
| Hyperparathyroidism Major signs | include osteoporosis, fractures, and kidney stones. Neuromuscular abnormalities are muscle weakness in proximal muscles of lower extremities. |
| Parathyroidectomy | leads to a reduction in chronically high calcium levels. |
| Hyperparathyroidism | Continued ambulation, avoidance of immobility, a high fluid intake and moderate calcium intake are important. |
| Several drugs are helpful in lowering calcium levels: | bisphosphonates (e.g., alendronate [Fosamax]) estrogen or progestin therapy, oral phosphate, diuretics, and calcimimetic agents (e.g., cinacalcet [Sensipar]). |
| Hypoparathyroidism | is rare, and results from inadequate circulating PTH. |
| Hypoparathyroidism is characterized by | hypocalcemia resulting from a lack of PTH to maintain serum calcium levels. |
| Hypoparathyroidism The most common cause | is iatrogenic, due to accidental removal of parathyroid glands or damage to these glands during neck surgery. |
| Sudden decreases in serum calcium | cause tetany,which is chara by tingling of lips,fingertips,inc muscle tension w/paresthesias &stiffness.Painful tonic spasms of smooth & skeletal muscles(extremities and face),laryngospasms &pos Chvostek sign & Trousseau sign are usually present |
| Hypoparathyroidism Focus of patient care | is to treat tetany, maintain normal serum calcium levels, and prevent long-term complications. Emergency treatment of tetany requires IV calcium.Instruction about lifelong treatment and follow-up care includes monitoring of calcium levels. |
| Cushing syndrome | is a spectrum of clinical abnormalities caused by excessive corticosteroids, particularly glucocorticoids. |
| Cushing syndrome The most common cause | is iatrogenic administration of exogenous corticosteroids (e.g., prednisone). |
| Most cases of endogenous Cushing syndrome | are due to adrenocorticotrophic hormone (ACTH) secreting pituitary tumor (Cushing’s disease). |
| Cushing syndrome Key signs | include centripedal or generalized obesity, “moon facies” (fullness of face), purplish red striae below the skin surface, hirsutism in women, hypertension, and unexplained hypokalemia. |
| Cushing syndrome Treatment | is dependent on the underlying cause, and includes surgery and drug therapy to normalize hormone levels. |
| Cushing syndrome Discharge instructions | are based on patient’s lack of endogenous corticosteroids and resulting inability to react to stressors physiologically. Lifetime replacement therapy is required by many patients. |
| In the patient with Addison’s disease, | all three classes of adrenal corticosteroids (glucocorticoids, mineralocorticoids, and androgens) are reduced. |
| Addison’s disease etiology | is mostly autoimmune where adrenal cortex is destroyed by autoantibodies. |
| Addison’s disease Manifestations | have a slow onset and include weakness, weight loss, and anorexia. |
| Addison’s disease Skin hyperpigmentation | is seen in sun-exposed areas of body, at pressure points, over joints, and in palmar creases. |
| Addison’s disease treatment | is replacement therapy. Hydrocortisone, the most commonly used form of replacement therapy, has both glucocorticoid and mineralocorticoid properties. During times of stress, glucocorticoid dosage is increased to prevent addisonian crisis. |
| Mineralocorticoid replacement | with fludrocortisone acetate (Florinef) is given daily with increased dietary salt. Patient teaching covers medications, techniques for stress management, and that patient must always wear an identification bracelet (Medic Alert). |
| Addisonian Crisis | Patients with Addison’s disease are at risk for an acute adrenal insufficiency (addisonian crisis), a life-threatening emergency caused by insufficient or sudden decrease in adrenocortical hormones. |
| Addisonian crisis | is triggered by stress (e.g., surgery, trauma, hemorrhage, or psychologic distress); sudden withdrawal of corticosteroid hormone replacement therapy; and post-adrenal surgery. |
| Addisonian Crisis Manifestations | include postural hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion. |
| Addisonian Crisis Treatment | is shock management and high-dose hydrocortisone replacement. Large volumes of 0.9% saline solution and 5% dextrose are given to reverse hypotension and electrolyte imbalances until blood pressure normalizes. |
| The use of long-term corticosteroids | in therapeutic doses often leads to serious complications and side effects. |
| LONG-TERM ADMINISTRATION OF CORTICOSTEROIDS Therapy | is reserved for diseases in which there is a risk of death or permanent loss of function, and conditions in which short-term therapy is likely to produce remission or recovery. |
| LONG-TERM ADMINISTRATION OF CORTICOSTEROIDS potential treatment | benefits must always be weighed against risks. |
| danger of abrupt cessation of corticosteroid therapy | must be emphasized to patients and significant others.Corticosteroids taken longer than 1 week will suppress adrenal production and oral corticosteroids should be tapered. |
| Nurses must ensure that increased doses of corticosteroids | are prescribed in acute care or home care situations with increased physical or emotional stress. |
| Hyperaldosteronism | is characterized by excessive aldosterone secretion commonly caused by small solitary adrenocortical adenoma. |
| Hyperaldosteronism main effects | are sodium retention and potassium and hydrogen ion excretion. |
| Hyperaldosteronism key sign of this disease | is hypertension with hypokalemic alkalosis. |
| Hyperaldosteronism preferred treatment | is surgical removal of adenoma (adrenalectomy). |
| Hyperaldosteronism Patients with bilateral adrenal hyperplasia | are treated with drugs. Calcium channel blockers may be used to control BP. Patients are taught to monitor own BP and need for monitoring. |
| Pheochromocytoma | is a rare condition characterized by an adrenal medulla tumor that produces excessive catecholamines (epinephrine, norepinephrine). |
| Pheochromocytoma tumor | is benign in most cases. |
| Pheochromocytoma secretion of excessive catecholamines | results in severe hypertension. |
| If undiagnosed and untreated, pheochromocytoma | may lead to diabetes mellitus, cardiomyopathy, and death. |
| Pheochromocytoma Manifestations | include severe, episodic hypertension accompanied by classic triad of (1) severe, pounding headache, (2) tachycardia with palpitations and profuse sweating, and (3) unexplained abdominal or chest pain. |
| Pheochromocytoma Attacks | may be provoked by many medications, including antihypertensives, opioids, radiologic contrast media, and tricyclic antidepressants. |
| Pheochromocytoma treatment | consists of surgical removal of tumor. |
| Chapter 40: | Nursing Management: Nutritional Problems |
| Good nutrition | in the absence of any underlying disease process results from the ingestion of a balanced diet. |
| The MyPyramid (formerly the Food Guide Pyramid) | consists of food groups that are presented in proportions appropriate for a healthy diet, including grains, vegetables, fruits, oils, milk, and meat and beans. |
| The National Research Council | recommends that at least half of the body’s energy needs should come from carbohydrates, especially complex carbohydrates. |
| The Dietary Guidelines for Americans 2005 from Healthy People 2010 | recommends that people reduce their fat intake to 20% to 35% of their total daily caloric intake. |
| An average adult requires | an estimated 20 to 35 calories per kilogram of body weight per day, leaning toward the higher end if the person is critically ill or very active and the lower end if the person is sedentary. |
| The recommended daily protein intake | is 0.8 to 1 g/kg of body weight. |
| Vegetarians can have vitamin or protein deficiencies | unless their diets are well planned. |
| Culture, personal preferences, socioeconomic status, and religious preferences | can influence food choices. |
| The nurse should include cultural and ethnic considerations | when assessing the patient’s diet history and implementing interventions that require dietary changes. |
| Malnutrition | is common in hospitalized patients.With starvation, the body initially uses carbohydrates (glycogen) rather than fat and protein to meet metabolic needs. Once carbohydrate stores are depleted, protein begins to be converted to glucose for energy. |
| Factors that contribute to malnutrition | include socioeconomic status, cultural influences, psychologic disorders, medical conditions, and medical treatments. |
| Regardless of the cause of the illness, most sick persons have | increased nutritional needs. |
| Each degree of temperature increase on the Fahrenheit scale raises | the basal metabolic rate (BMR) by about 7%. |
| Prolonged illness, major surgery, sepsis, draining wounds, burns, hemorrhage, fractures, and immobilization can | all contribute to malnutrition. |
| On physical examination, the most obvious clinical signs of inadequate protein and calorie intake are | apparent in the skin, eyes, mouth, muscles, and the central nervous system. |
| The malnourished person | is more susceptible to all types of infection. |
| Across all settings of care delivery, the nurse must be aware of | the nutritional status of the patient. |
| The protein and calorie intake | required in the malnourished patient depends on the cause of the malnutrition, the treatment being employed, and other stressors affecting the patient. |
| The older patient is at risk for nutritional problems due to the following factors: | Changes in the oral cavity, Changes in digestion and motility, Changes in the endocrine system, Changes in the musculoskeletal system, Decreases in vision and hearing |
| High-calorie oral supplements may be used in the patient whose | nutritional intake is deficient. |
| Tube feeding (also known as enteral nutrition) | may be ordered for the patient who has a functioning GI tract but is unable to take any or enough oral nourishment. |
| A gastrostomy tube | may be used for a patient who requires tube feedings over an extended time. |
| The most accurate assessment for correct tube placement | is by x-ray visualization. |
| Parenteral nutrition (PN) | is used to meet the patient’s nutritional needs and to allow growth of new body tissue. |
| All parenteral nutrition solutions | should be prepared by a pharmacist or a trained technician using strict aseptic techniques under a laminar flow hood. |
| Complications of parenteral nutrition include | infectious, metabolic, and mechanical problems. |
| Chapter 25: | Nursing Management: Burns |
| Burns | are body tissue injuries due to heat, cold, chemicals, electrical current, or radiation. |
| Smoke and inhalation injuries | result from inhalation of hot air or noxious chemicals. |
| The resulting effect of burns | is influenced by the temperature of the burning agent, the duration of contact time, and the tissue type injured. |
| Burn prevention programs | focus on child-resistant lighters; nonflammable children’s clothing; stricter building codes; smoke detectors/alarms; and fire sprinklers. |
| Nurses need to advocate | for scald- and fire risk–reduction strategies in the home. Occupational health nurses need to educate workers to reduce scald, chemical, electrical, and thermal injuries in the work setting. |
| Burn treatment | is related to injury severity determined by depth. The extent is calculated by the percent of the total body surface area (TBSA), location, and patient risk factors. |
| Burns are defined by | degrees: first degree (same as sunburn), second degree, and third degree. A more precise definition of second- and third-degree burns includes the depth of skin destruction: partial-thickness and full-thickness. |
| Second- and third-degree burn | extent can be determined using total body surface area based on two guides: Lund-Browder chart and Rule of Nines. Burn extent is often revised after edema subsides and demarcation of injury zones occurs. |
| Face, neck, and circumferential burns | to the chest/back area may inhibit respiratory function with mechanical obstruction secondary to edema or leathery, devitalized tissue (eschar) formation. These injuries may cause inhalation injury and respiratory mucosal damage. |
| Hands, feet, and eye burns may make | self-care difficult and jeopardize future function. Buttocks or genitalia burns are susceptible to infection. Circumferential burns to extremities can cause circulatory compromise distal to the burn. |
| Burn management | is organized chronologically into three phases: emergent (resuscitative), acute (wound healing), and rehabilitation (restorative). Overlaps in care exist from one phase to another. |
| EMERGENT PHASE | Period of time required to resolve immediate, life-threatening problems. Phase may last from time of burn to 3 or more days, but it usually lasts 24 to 48 hours. |
| EMERGENT PHASE primary concern | onset of hypovolemic shock&edema formation. Toward end of phase,if fluid replacement is adequate,capillary membrane permeability is restored.Fluid loss &edema cease.interstitial fluid returns to vascular.Diuresis occurs w/low urine specific gravities |
| EMERGENT PHASE Manifestations | include shock from the pain and hypovolemia. Areas of full-thickness and deep partial-thickness burns are initially anesthetic because the nerve endings are destroyed. Superficial to moderate partial-thickness burns are painful. |
| EMERGENT PHASE Shivering occurs | as a result of chilling, and most patients are alert. Unconsciousness or altered mental status is usually a result of hypoxia associated with smoke inhalation, head trauma, or excessive sedation or pain medication. |
| EMERGENT PHASE Complications: | CV:dysrhythmias&hypovolemic shock,Resp:U airway injury W/edema formation&obstruction,inhalation injury Renal:blood flow dec,renal ischemia.acute renal failure.fullthickness&electrical burns,myoglobin&hgb are released into bloodstream&occlude renal tubules |
| EMERGENT PHASE Management | includes a rapid and thorough assessment and intervention of airway management, fluid therapy, and wound care. Analgesics are ordered to promote patient comfort. Early in the postburn period, IV pain medications are given. |
| EMERGENT PHASE Early and aggressive nutritional support | decreases mortality and complications, optimizes healing of burn, and minimizes negative effects of hypermetabolism and catabolism. |
| ACUTE PHASE | Begins with the mobilization of extracellular fluid and subsequent diuresis. Phase concludes when burned area is completely covered by skin grafts or when wounds are healed. This may take weeks or many months. |
| ACUTE PHASE Manifestations | include eschar from partial-thickness wounds. Once removed, re-epithelialization appears as red or pink scar tissue.Margins of full-thickness eschar take longer to separate. As a result, they require surgical debridement and skin grafting for healing. |
| ACUTE PHASE Because the body is trying to reestablish fluid and electrolyte homeostasis, | it is important for the nurse to follow the patient’s serum electrolyte levels closely (hypo- or hypernatremia, hypo- or hyperkalemia). |
| ACUTE PHASE Complications | include wound infection progressing to transient bacteremia as result of manipulation (e.g., after hydrotherapy and debridement). Same cardiovascular and respiratory system complications as in emergent phase may continue. |
| ACUTE PHASE | Pt can become extremely disoriented, withdraw, or combative. transient state, lasting from a day to several weeks. Range of motion may be limited and contractures can occur. Paralytic ileus results from sepsis. Diarrhea and constipation may also occur. |
| ACUTE PHASE Management | involves wound care with daily observation, assessment, cleansing, debridement, and dressing reapplication. |
| ACUTE PHASE Individualized and consistent pain assessment and care are essential. | Note two kinds of pain: continuous, background pain existing throughout day and night, and treatment pain associated with dressing changes, ambulation, and rehabilitation activities. |
| ACUTE PHASE First line of treatment | pharmacologic. Then nonpharmacologic strategies:relaxation tapes,visualization,hypnosis,guided imagery,biofeedback.Rigorous physical through recovery imperative to joint function.Nutritional provides adequate calories &protein to promote healing |
| REHABILITATION PHASE | Begins when wounds have healed and patient is able to resume self-care activity. Phase occurs as early as 2 weeks or as long as 7 to 8 months after the burn. |
| REHABILITATION PHASE Goals | are to assist the patient in resuming a functional role in society and accomplish functional and cosmetic reconstructive surgery. |
| REHABILITATION PHASE Manifestations | include new skin appearing flat and pink, then raised and hyperemic; itching occurs with healing. Complications are skin and joint contractures and hypertrophic scarring. |
| REHABILITATION PHASE Management | positioning,splinting,exercise to minimize contracture. Burned legs may be wrapped w/elastic(tensor/Ace)to assist circulation to leg graft/donor sites. Patient education and “hands-on” instruction need to be provided in dressing changes and wound care. |
| REHABILITATION PHASE Continuous exercise and physical/occupational therapy | cannot be overemphasized. Encouragement and reassurance are necessary for patient morale, attaining independence, and returning to preburn activities. |
| REHABILITATION PHASE For patient with emotional needs, | it is important that the nurse have understanding of circumstances of burn, family relationships, and prior coping experiences with stressful situations. Patient may experience fear, anxiety, anger, guilt, and depression. |
| Chapter 44: | Nursing Management: Liver, Pancreas, and Biliary Tract Problems |
| Jaundice | a yellowish discoloration of body tissues, results from an alteration in normal bilirubin metabolism or flow of bile into the hepatic or biliary duct systems. |
| The three types of jaundice | are hemolytic, hepatocellular, and obstructive. |
| Hemolytic (prehepatic) jaundice | is due to an increased breakdown of red blood cells (RBCs), which produces an increased amount of unconjugated bilirubin in the blood. |
| Hepatocellular (hepatic) jaundice | results from the liver’s altered ability to take up bilirubin from the blood or to conjugate or excrete it. |
| Obstructive (posthepatic) jaundice | is due to decreased or obstructed flow of bile through the liver or biliary duct system. |
| Hepatitis | is an inflammation of the liver. Viral hepatitis is the most common cause of hepatitis. The types of viral hepatitis are A, B, C, D, E, and G. |
| Hepatitis A | is an RNA virus that is transmitted through the fecal-oral route. |
| The mode of transmission of HAV | is mainly transmitted by ingestion of food or liquid infected with the virus and rarely parenteral. |
| Hepatitis B | is a DNA virus that is transmitted perinatally by mothers infected with HBV; percutaneously (e.g., IV drug use); or horizontally by mucosal exposure to infectious blood, blood products, or other body fluids. |
| HBV is a complex structure | with three distinct antigens: the surface antigen (HBsAg), the core antigen (HBcAg), and the e antigen (HBeAg). |
| Approximately 6% of those infected when older than age 5 develop | chronic HBV. |
| Hepatitis C | is an RNA virus that is primarily transmitted percutaneously. |
| The most common mode of HCV | transmission is the sharing of contaminated needles and paraphernalia among IV drug users.There are 6 genotypes and more than 50 subtypes of HCV. |
| Hepatitis D virus (HDV) | is an RNA virus that cannot survive on its own. It requires HBV to replicate. |
| Hepatitis E virus (HEV) | is an RNA virus that is transmitted by the fecal-oral route. |
| Hepatitis G virus (HGV) | is a sexually transmitted virus. HGV coexists with other viral infections, including HBV, HCV, and HIV. |
| Hepatitis Clinical manifestations: | Many patients with hepatitis have no symptoms. |
| Hepatitis Symptoms of the acute phase | include malaise, anorexia, fatigue, nausea, occasional vomiting, and abdominal (right upper quadrant) discomfort. Physical examination may reveal hepatomegaly, lymphadenopathy, and sometimes splenomegaly. |
| Many HBV infections and the majority of HCV infections | result in chronic (lifelong) viral infection. |
| Most patients with acute viral hepatitis | recover completely with no complications. |
| Approximately 75% to 85% of patients who acquire HCV | will go on to develop chronic infection. |
| Fulminant viral hepatitis results | in severe impairment or necrosis of liver cells and potential liver failure. |
| There is no specific treatment or therapy for | acute viral hepatitis. |
| Drug therapy for chronic HBV and HBC | is focused on decreasing the viral load, aspartate aminotransferase (AST) and aspartate aminotransferase (ALT) levels, and the rate of disease progression. |
| Chronic HBV drugs | include interferon, lamivudine (Epivir), adefovir (Hepsera), entecavir (Baraclude), and telbivudine (Tyzeka). |
| Treatment for HCV includes | pegylated -interferon (Peg-Intron, Pegasys) given with ribavirin (Rebetol, Copegus). |
| Both hepatitis A vaccine and immune globulin (IG) | are used for prevention of hepatitis A. |
| Immunization with HBV vaccine | is the most effective method of preventing HBV infection. For postexposure prophylaxis, the vaccine and hepatitis B immune globulin (HBIG) are used. |
| Currently there is no vaccine to prevent | HCV. |
| Most patients with viral hepatitis will be cared for at home, so the nurse must assess | the patient’s knowledge of nutrition and provide the necessary dietary teaching. |
| Autoimmune hepatitis | is a chronic inflammatory disorder of unknown cause. It is characterized by the presence of autoantibodies, high levels of serum immunoglobulins, and frequent association with other autoimmune diseases. |
| Autoimmune hepatitis | (in which there is evidence of necrosis and cirrhosis) is treated with corticosteroids or other immunosuppressive agents. |
| Wilson’s disease | is a progressive, familial, terminal neurologic disease accompanied by chronic liver disease leading to cirrhosis.It is associated with increased storage of copper. |
| Primary biliary cirrhosis (PBC) | is characterized by generalized pruritus, hepatomegaly, and hyperpigmentation of the skin. |
| Nonalcoholic fatty liver disease (NAFLD) | is a group of disorders that is characterized by hepatic steatosis (accumulation of fat in the liver) that is not associated with other causes such as hepatitis, autoimmune disease, or alcohol. |
| The risk for developing NAFLD | is a major complication of obesity. NAFLD can progress to liver cirrhosis. |
| NAFLD should be considered in patients with risk factors | such as obesity, diabetes, hypertriglyceridemia, severe weight loss (especially in those whose weight loss was recent), and syndromes associated with insulin resistance. |
| Cirrhosis | is a chronic progressive disease characterized by extensive degeneration and destruction of the liver parenchymal cells. |
| Common causes of cirrhosis include | alcohol, malnutrition, hepatitis, biliary obstruction, and right-sided heart failure. Excessive alcohol ingestion is the single most common cause of cirrhosis followed by chronic hepatitis (B and C). |
| Manifestations of cirrhosis include | jaundice, skin lesions (spider angiomas), hematologic problems (thrombocytopenia, leucopenia, anemia, coagulation disorders), endocrine problems, and peripheral neuropathy. |
| Major complications of cirrhosis include | portal hypertension, esophageal and gastric varices, peripheral edema and ascites, hepatic encephalopathy, and hepatorenal syndrome. |
| Hepatic encephalopathy | is a neuropsychiatric manifestation of liver damage. It is considered a terminal complication in liver disease. |
| A characteristic symptom of hepatic encephalopathy | is asterixis (flapping tremors). |
| Diagnostic tests for cirrhosis include | elevations in liver enzymes, decreased total protein, fat metabolism abnormalities, and liver biopsy. |
| There is no specific therapy for cirrhosis. | Management of ascites is focused on sodium restriction, diuretics, and fluid removal. |
| Peritoneovenous shunt | is a surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system. |
| The main therapeutic goal for esophageal and gastric varices | is avoidance of bleeding and hemorrhage. |
| Transjugular intrahepatic portosystemic shunt (TIPS) | is a nonsurgical procedure in which a tract (shunt) between the systemic and portal venous systems is created to redirect portal blood flow. |
| Management of hepatic encephalopathy | is focused on reducing ammonia formation and treating precipitating causes. |
| An important nursing focus is | the prevention and early treatment of cirrhosis. |
| If the patient has esophageal and/or gastric varices in addition to cirrhosis, the nurse observes for any signs of | bleeding from the varices (e.g., hematemesis, melena). |
| The focus of nursing care of the patient with hepatic encephalopathy | is on maintaining a safe environment, sustaining life, and assisting with measures to reduce the formation of ammonia. |
| Fulminant hepatic failure, | or acute liver failure, is a clinical syndrome characterized by severe impairment of liver function associated with hepatic encephalopathy. |
| Indications for liver transplant include | chronic viral hepatitis, congenital biliary abnormalities (biliary atresia), inborn errors of metabolism, hepatic malignancy (confined to the liver), sclerosing cholangitis, fulminant hepatic failure, and chronic end-stage liver disease. |
| Postoperative complications of liver transplant include | rejection and infection. |
| The patient who has had a liver transplant requires | highly skilled nursing care. |
| Acute pancreatitis | is an acute inflammatory process of the pancreas. The primary etiologic factors are biliary tract disease (most common cause in women) and alcoholism (most common cause in men). |
| Abdominal pain usually located in the left upper quadrant | is the predominant symptom of acute pancreatitis. Other manifestations include nausea, vomiting, hypotension, tachycardia, and jaundice. |
| Two significant local complications of acute pancreatitis | are pseudocyst and abscess. A pancreatic pseudocyst is a cavity continuous with or surrounding the outside of the pancreas. |
| The primary diagnostic tests for acute pancreatitis | are serum amylase and lipase. |
| Objectives of collaborative care for acute pancreatitis | include relief of pain; prevention or alleviation of shock; reduction of pancreatic secretions; control of fluid and electrolyte imbalances; prevention or treatment of infections; and removal of the precipitating cause. |
| Because hypocalcemia can also occur, the nurse must observe for symptoms of | tetany, such as jerking, irritability, and muscular twitching. |
| Chronic pancreatitis | is a continuous, prolonged, inflammatory, and fibrosing process of the pancreas. The pancreas becomes progressively destroyed as it is replaced with fibrotic tissue. Strictures and calcifications may also occur in the pancreas. |
| Clinical manifestations of chronic pancreatitis include | abdominal pain, symptoms of pancreatic insufficiency, including malabsorption with weight loss, constipation, mild jaundice with dark urine, steatorrhea, and diabetes mellitus. |
| Measures used to control the pancreatic insufficiency | include diet, pancreatic enzyme replacement, and control of the diabetes. |
| The majority of pancreatic cancers | have metastasized at the time of diagnosis. The signs and symptoms of pancreatic cancer are often similar to those of chronic pancreatitis. |
| Transabdominal ultrasound and CT scan are the most commonly used diagnostic imaging techniques for | pancreatic diseases, including cancer. |
| Surgery provides the most effective treatment of cancer of the pancreas; | however, only 15% to 20% of patients have resectable tumors. |
| The most common disorder of the biliary system | is cholelithiasis (stones in the gallbladder). Cholecystitis (inflammation of the gallbladder) is usually associated with cholelithiasis. |
| Ultrasonography is commonly used to diagnose | gallstones. |
| Medical dissolution therapy | is recommended for patients with small radiolucent stones who are mildly symptomatic and are poor surgical risks. |
| Cholelithiasis | develops when the balance that keeps cholesterol, bile salts, and calcium in solution is altered and precipitation occurs. Ultrasonography is commonly used to diagnose gallstones. |
| Initial symptoms of acute cholecystitis | include indigestion and pain and tenderness in the right upper quadrant. |
| Complications of cholecystitis | include gangrenous cholecystitis, subphrenic abscess, pancreatitis, cholangitis (inflammation of biliary ducts), biliary cirrhosis, fistulas, and rupture of the gallbladder, which can produce bile peritonitis. |
| Postoperative nursing care following a laparoscopic cholecystectomy | includes monitoring for complications such as bleeding, making the patient comfortable, and preparing the patient for discharge. |
| The nurse should assume responsibility for recognition of predisposing factors | of gallbladder disease in general health screening. |
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